Inflammation has become a central theme in the pathogenesis of cardiovascular disease over the past decade, and a wide range of cardiac diseases has been associated with inflammation and cytokine modulation (Mehra et al., 2005, J. Leukocyte Biol. 78:805-818). Proinflammatory cytokines may be secreted by every nucleated cell type in the myocardium, including the cardiac myocyte, in response to various forms of stress/injury. They are elevated in conditions as diverse as inflammatory myocarditis, allograft rejection, cardiac ischemic states, congestive heart failure (CHF), and reperfusion injury.
IL-1β is a pro-inflammatory cytokine secreted by a number of different cell types including monocytes and macrophages. When released as part of an inflammatory reaction, IL-1β produces a range of biological effects, mainly mediated through induction of other inflammatory mediators such as corticotrophin, platelet factor-4, prostaglandin E2 (PGE2), IL-6, and IL-8. IL-1β induces both local and systemic inflammatory effects through the activation of the IL-1 receptor found on almost all cell types. The interleukin-1 (IL-1) family of cytokines has been implicated in a number of disease states. IL-1 family members include IL-1α, IL-1β, and IL-1Ra. Although related by their ability to bind to IL-1 receptors (IL-1R1 and IL-1R2), each of these cytokines is different, being expressed by a different gene and having a different primary amino acid sequence. Furthermore, the physiological activities of these cytokines can be distinguished from each other.